Anticentromere antibodies (ACA) were associated with lower oocyte maturation rates and cleavage rates, while the mechanism was not clear. Aims of this study were to examine whether active immunization with centromere protein C could elicit the CENP-C autoantibody in mice and the impacts of the CENP-C autoantibody on oocyte meiosis. Mice were divided into two groups, one was the experimental group immunized with human centromere protein C and Freund’s adjuvant (CFA), and the other was the control group injected with CFA only. Serum and oocytes of BALB/c mice immunized with human centromere protein C (CENP-C) in complete Freund’s adjuvant (CFA) or injected with only CFA were studied for the development of the CENP-C antibody. Rates of germinal vesicle breakdown (GVBD), first polar body (Pb1) extrusion, abnormal spindle morphology, and chromosome misalignment were compared between the experimental group and the control group. The CENP-C antibody was only observed in serum and oocytes of mice immunized with the centromere protein C antigen. The first polar body (Pb1) extrusion rate was lower in the experimental group (). A higher percentage of spindle defects and chromosome congression failure were also detected in the experimental group (spindle defects: vs. control; chromosome misalignment: vs. control; for both). Oocyte meiosis was severely impaired by the CENP-C antibody, which may be the main mechanism of adverse reproductive outcomes for ACA-positive women who have no clinical symptoms of any autoimmune diseases.

中文翻译：

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CENP-C 免疫导致小鼠卵母细胞减数分裂期间染色体分离异常

抗着丝粒抗体（ACA）与较低的卵母细胞成熟率和卵裂率有关，但机制尚不清楚。本研究的目的是检查用着丝粒蛋白 C 主动免疫是否可以在小鼠中引发 CENP-C 自身抗体以及 CENP-C 自身抗体对卵母细胞减数分裂的影响。小鼠分为两组，一组为接种人着丝粒蛋白C和弗氏佐剂（CFA）的实验组，另一组为仅注射CFA的对照组。研究了用完全弗氏佐剂 (CFA) 中的人着丝粒蛋白 C (CENP-C) 免疫或仅注射 CFA 的 BALB/c 小鼠的血清和卵母细胞，以开发 CENP-C 抗体。生发囊泡破裂 (GVBD)、第一极体 (Pb1) 挤出、纺锤体形态异常、比较实验组和对照组的染色体错位情况。CENP-C 抗体仅在用着丝粒蛋白 C 抗原免疫的小鼠的血清和卵母细胞中观察到。实验组的第一极体（Pb1）挤出速率较低（）。在实验组中还检测到更高百分比的纺锤体缺陷和染色体大会失败（纺锤体缺陷： 对比 控制; 染色体错位： 对比 控制; 对彼此而言）。CENP-C抗体严重损害了卵母细胞减数分裂，这可能是没有任何自身免疫性疾病临床症状的ACA阳性女性出现不良生殖结局的主要机制。